Chlorella viruses evoke a rapid release of K+ from host cells during the early phase of infection

Neupärtl, Monika; Meyer, Christine; Woll, Isabell; Frohns, Florian; Kang, Ming; Etten, James L. Van; Krämer, D.; Hertel, Brigitte; Moroni, Anna; Thiel, Gerhard

doi:10.1016/j.virol.2007.10.024

Cited by 45 publications

(47 citation statements)

References 39 publications

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“…Moroni, G. Thiel, and B. Hertel, unpublished data) that leads to the rapid depolarization of the host plasma membrane (Frohns et al, 2006). Potassium ions are released rapidly from the infected cells (Neupärtl et al, 2008), and this lowers the turgor pressure of the cell, which is hypothesized to aid the transfer of DNA from the virus particle into the host. Virus infection is inhibited by the same compounds that block channel function in heterologous systems (Mehmel et al, 2003;Frohns et al, 2006).…”

Section: Viral Channel Evolution Is Driven By Selection Pressurementioning

confidence: 99%

Potassium Ion Channels: Could They Have Evolved from Viruses?

et al. 2013

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Section: Viral Channel Evolution Is Driven By Selection Pressurementioning

confidence: 99%

Potassium Ion Channels: Could They Have Evolved from Viruses?

et al. 2013

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“…As mentioned in the introduction, the virus-encoded K ϩ channel protein (Kcv) is predicted to be responsible for cell membrane depolarization during virus infection. Chlorovirus-encoded Kcv channels have selective sensitivity to known K ϩ channel blockers (24,28 …”

Section: Effect Of Virus Infection On Adenine Uptakementioning

confidence: 99%

“…The addition of PBCV-1 to its host, Chlorella strain NC64A, leads to the following program of events: (i) virus attachment to the cell wall is host specific and occurs at a unique virus vertex (45), followed by wall degradation at the point of attachment (25); (ii) rapid host membrane depolarization (11) and potassium ion release (28) occur within minutes of virus attachment; (iii) host nuclear DNA degradation begins at 3 to 5 min postinfection (p.i.) (1); (iv) early viral transcripts begin to appear at 5 to 10 min p.i.…”

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confidence: 99%

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Chlorovirus-Mediated Membrane Depolarization ofChlorellaAlters Secondary Active Transport of Solutes

Agarkova

Dunigan

Gurnon

et al. 2008

J Virol

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Paramecium bursaria chlorella virus 1 (PBCV-1) is the prototype of a family of large, double-stranded DNA, plaque-forming viruses that infect certain eukaryotic chlorella-like green algae from the genus Chlorovirus. PBCV-1 infection results in rapid host membrane depolarization and potassium ion release. One interesting feature of certain chloroviruses is that they code for functional potassium ion-selective channel proteins (Kcv) that are considered responsible for the host membrane depolarization and, as a consequence, the efflux of potassium ions. This report examines the relationship between cellular depolarization and solute uptake. Annotation of the virus host Chlorella strain NC64A genome revealed 482 putative transporter-encoding genes; 224 are secondary active transporters. Solute uptake experiments using seven radioactive compounds revealed that virus infection alters the transport of all the solutes. However, the degree of inhibition varied depending on the solute. Experiments with nystatin, a drug known to depolarize cell membranes, produced changes in solute uptake that are similar but not identical to those that occurred during virus infection. Therefore, these studies indicate that chlorovirus infection causes a rapid and sustained depolarization of the host plasma membrane and that this depolarization leads to the inhibition of secondary active transporters that changes solute uptake.

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“…brane depolarization (9), potassium ion efflux (25), and an increase in the cytoplasm pH (2). These events are predicted to facilitate entry of the viral DNA and virion-associated proteins into the cell.…”

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Microarray Analysis of Paramecium bursaria Chlorella Virus 1 Transcription

Yanai-Balser

Duncan

Eudy

et al. 2010

J Virol

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Paramecium bursaria chlorella virus 1 (PBCV-1), the prototype of the genus Chlorovirus (family Phycodnaviridae), is a large, icosahedral (190 nm in diameter), plaque-forming virus that infects the unicellular, eukaryotic green alga Chlorella sp. strain NC64A. The PBCV-1 virion has a lipid membrane located inside an outer glycoprotein capsid. The 330-kb genome is a linear, nonpermutated, double-stranded DNA (dsDNA) molecule with covalently closed hairpin ends that has approximately 365 protein encoding genes (CDSs), as well as 11 tRNA encoding genes (reviewed in references 34, 39, and 40). The CDSs are evenly distributed on both strands and intergenic space is minimal (typically fewer than 100 nucleotides); the exception is a 1,788-bp sequence in the middle of the genome that encodes the tRNA genes. Approximately 35% of the 365 PBCV-1 gene products resemble proteins in the public databases.PBCV-1 initiates infection by attaching rapidly and specifically to the cell wall of its host (22), probably at a unique virus vertex (4, 26). Attachment is immediately followed by host cell wall degradation by a virus-packaged enzyme(s) at the point of contact. After wall degradation, the viral internal membrane presumably fuses with the host membrane, causing host membrane depolarization (9), potassium ion efflux (25), and an increase in the cytoplasm pH (2). These events are predicted to facilitate entry of the viral DNA and virion-associated proteins into the cell. PBCV-1 lacks a gene encoding a recognizable RNA polymerase or a subunit of it, and RNA polymerase activity is not detected in PBCV-1 virions. Therefore, viral DNA and virion-associated proteins are predicted to migrate to the nucleus, and early viral transcription is detected 5 to 10 min postinfection (p.i.), presumably by commandeering a host RNA polymerase(s) (possibly RNA polymerase II) (14, 29). Virus DNA synthesis begins 60 to 90 min p.i., followed by virus assembly at 3 to 5 h p.i. in localized regions of the cytoplasm, called virus assembly centers (21). At 6 to 8 h p.i., virusinduced host cell lysis occurs resulting in release of progeny virions (ϳ1,000 viruses/cell, ϳ25% of which are infectious). These events are depicted in Fig. 1.To initiate PBCV-1 transcription, the host RNA polymerase(s), possibly in combination with a virus transcription factor(s), must recognize virus DNA promoter sequences. Recently, three short nucleotide sequences were identified in putative virus promoter regions (150 bp upstream and 50 bp downstream of the ATG translation site) that are conserved in PBCV-1 and other Chlorovirus members (7). PBCV-1 CDSs are not spatially clustered on the genome by either temporal or functional class, suggesting that transcription regulation must occur via cis-and possible trans-acting regulatory elements.To understand the dynamics of PBCV-1 global gene expression during virus replication, we constructed a microarray containing 50-mer probes to each of the 365 PBCV-1 CDSs.

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Chlorella viruses evoke a rapid release of K+ from host cells during the early phase of infection

Cited by 45 publications

References 39 publications

Potassium Ion Channels: Could They Have Evolved from Viruses?

Potassium Ion Channels: Could They Have Evolved from Viruses?

Chlorovirus-Mediated Membrane Depolarization ofChlorellaAlters Secondary Active Transport of Solutes

Microarray Analysis of Paramecium bursaria Chlorella Virus 1 Transcription

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